Defining a role for the homeoprotein Six1 in EMT and mammary tumorigenesis.
Defining a role for the homeoprotein Six1 in EMT and mammary tumorigenesis.
复制标题
DOI：
10.1172/jci40555
复制
发表时间：
2009-09
期刊：
影响因子：
--
通讯作者：
D. Radisky
中科院分区：
文献类型：
--
作者：
D. Radisky
同源盒（Hox）基因编码转录因子，这些转录因子是胚胎发生期间生长和分化的关键调节因子。虽然许多研究已经确定Hox基因在肿瘤中的表达增加，但对Hox基因促进肿瘤发展的机制基础知之甚少。在本期《JCI》中，麦考伊及其同事表明，在乳腺上皮细胞中表达同源蛋白Six 1的转基因小鼠显示干/祖细胞群增加，随后出现肿瘤发展，而在另一项研究中，Micalizzi及其同事发现Six 1的过表达通过诱导上皮-间质转化（EMT）促进乳腺癌细胞转移，（分别参见2663页和2678页开始的相关文章）。他们的发现暗示Six 1是乳腺癌发展的中心介质。
Homeobox (Hox) genes encode transcription factors that act as critical regulators of growth and differentiation during embryogenesis. While many studies have identified increased expression of Hox genes in tumors, much less is known about the mechanistic basis by which Hox genes facilitate tumor development. In this issue of the JCI, McCoy and colleagues show that transgenic mice that express the homeoprotein Six1 in mammary epithelial cells show increases in stem/progenitor cell populations and subsequent tumor development, while in a separate study Micalizzi and colleagues show that overexpression of Six1 facilitates breast cancer cell metastasis by inducing epithelial-mesenchymal transition (EMT) (see the related articles beginning on pages 2663 and 2678, respectively). Their findings implicate Six1 as a central mediator of breast cancer development.